Mutations in the RAS family of small GTPases occur in approximately one‐fifth of all human cancers.[1] Kirsten rat sarcoma viral oncogene homolog (KRAS) is the most frequently mutated member, with an especially high mutation rate in pancreatic adenocarcinoma (PDAC), and a notable incidence in appendiceal adenocarcinoma, small bowel adenocarcinoma, colorectal cancer (CRC), and nonsmall cell lung cancer (NSCLC) (Figure1).[2] This underscores the significant therapeutic demand for effective KRAS inhibitors. This evidence concerns the gene KRAS and colorectal cancer.